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The distribution of these receptors was also similar to that of glucagon receptors

Mohammad Flood
· 3 min read
The distribution of these receptors was also similar to that of glucagon receptors

The thalamus-hypothalamus, pituitary gland, and medulla oblongata were rich in GLP-1 and glucagon-binding sites. The binding affinities of GLP-1 and glucagon were in the nanomolar range [disocciation constant Kd approximately equal to 4 nM]. The presence of specific, high affinity receptors for GLP-1 was confirmed by demonstrating that GLP-1 stimulated cAMP formation in the thalamus-hypothalamus and the pituitary gland. The concentration of GLP-1 required for half-maximal stimulation of cAMP formation in these regions was about 1 nM.  glp 1 meds  suggest that GLP-1 may be synthesized in certain parts of the brain and play a role as a neurosignal transmitter.Liraglutide Improves the Kidney Function in a Murine Model of Chronic Kidney BACKGROUND: Chronic kidney disease (CKD) is a global health burden, and the current treatment options only slow down the disease progression.

GLP-1 receptor agonists (GLP-1 RA) have shown a renal protective effect in models of CKD; however, the mechanism behind the beneficial effect is not understood. In this study, we investigate the effect of the GLP-1 RA liraglutide in the nephrotoxic serum nephritis (NTN) CKD model. Moreover,  glipizide used for  compare the gene expression pattern of liraglutide-treated mice to the gene expression pattern of mice treated with the angiotensin converting enzyme inhibitor, enalapril.METHODS: The effect of liraglutide was tested in the NTN model by evaluating the glomerular filtration rate (GFR), albuminuria, mesangial expansion, renal fibrosis, and renal inflammation. Furthermore, the regulation of selected genes involved in CKD and in glomerular, cortical tubulointerstitial, and whole kidney structures was analyzed using a gene expression array on samples following laser RESULTS: Treatment with liraglutide improved CKD hallmarks including GFR, albuminuria, mesangial expansion, renal inflammation, and renal fibrosis. The gene expression revealed that both liraglutide and enalapril reversed the regulation of several fibrosis and inflammation associated genes, which are also regulated in human CKD patients. Furthermore, liraglutide and enalapril both regulated genes in the kidney involved in blood pressure control.

CONCLUSIONS: Treatment with liraglutide improved the kidney function and diminished renal lesions in NTN-induced mice. Both liraglutide and enalapril reversed the regulation of genes involved in CKD and regulated genes involved in Efficacy and safety of once-weekly semaglutide 1mg vs once-daily liraglutide 1mg as add-on to 1-3 oral antidiabetic drugs in subjects with type 2 diabetes Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.AIMS: SUSTAIN 10 compared the efficacy and safety of the anticipated most frequent semaglutide dose (1mg) with the current most frequently prescribed liraglutide dose in Europe (1mg), reflecting clinical practice.METHODS: In this phase 3b, open-label trial, 577 adults with type 2 diabetes (HbA1c 7-11%) on 1-3 oral antidiabetic drugs were randomized 1:1 to subcutaneous once-weekly semaglutide 1mg or subcutaneous once-daily liraglutide 1mg. Primary and confirmatory secondary endpoints were changes in HbA1c and body weight from baseline to week 30, respectively.RESULTS: Mean HbA1c (baseline 8%) decreased by 1% with semaglutide and 1% with liraglutide (estimated treatment difference [ETD] -09%; 95% confidence interval [CI] -02 to -06, P<0001). Mean body weight (baseline 96kg) decreased by 5kg with semaglutide and 1kg with liraglutide (ETD -33kg; 95% CI -47 to -39, P<0001).

The proportions of subjects achieving glycaemic targets of<7% and=6%, weight loss of=5% and=10%, and a composite endpoint of HbA1c<7% without severe or blood glucose-confirmed symptomatic hypoglycaemia and no weight gain were greater with semaglutide vs liraglutide (all P<0001). Both treatments had similar safety profiles, except for more frequent gastrointestinal disorders (the most common adverse events [AEs]) and AEs leading to premature treatment discontinuation with semaglutide vs liraglutide (43% vs 38% and 11% vs 6%, respectively).CONCLUSION: Semaglutide was superior to liraglutide in reducing HbA1c and body weight. Safety profiles were generally similar, except for higher rates of gastrointestinal AEs with semaglutide vs liraglutide.Effects of chronic treatment with metformin on dipeptidyl peptidase-4 activity, glucagon-like peptide 1 and ghrelin in obese patients with Type 2 diabetes AIMS: Studies investigating the acute effects of metformin have demonstrated actions on the incretin system and appetite regulatory hormones. There are limited data to support that these effects are sustained in the long term. We therefore studied the effects of chronic treatment with metformin on endogenous glucagon-like peptide 1, dipeptidyl peptidase-4 activity and active ghrelin (an orexigenic hormone) in obese patients with Type 2 diabetes mellitus.

, HbA(1c) 69 ± 6 mmol/mol (8 ± 0%), mean ± sem] with drug-naïve Type 2 diabetes were studied for 6 h following a standard mixed meal, before and after at least 3 months of metformin monotherapy (mean dose 15 g daily).RESULTS: The area under the curve (AUC(0-6 h) ) for active glucagon-like peptide 1 was significantly higher on metformin (pre-metformin 1750 ± 640 pmol l(-1) min(-1) vs. post-metformin 2718 ± 1182 pmol l(-1) min(-1) ; P=01).